Targeting ferroptosis in cervical cancer: Mechanistic insights and therapeutic opportunities

Cervical cancer is the fourth most common malignancy among women worldwide. Despite standard chemoradiotherapy, a significant number of patients experience recurrence or distant metastasis. Accumulating evidence highlights ferroptosis-an iron-dependent form of regulated cell death driven by lipid peroxidation (LPO)-as a key mechanism influencing cervical carcinogenesis and treatment outcomes. Ferroptosis is marked by intracellular iron overload, excessive reactive oxygen species (ROS) production, and loss of redox balance. This review provides a comprehensive overview of the emerging roles of ferroptosis in the initiation, progression, and therapeutic resistance of cervical cancer. We outline the regulatory networks and signaling pathways that control ferroptosis in cervical cancer cells and assess the therapeutic potential of inducing ferroptosis using small-molecule compounds and nanomedicine approaches. Additionally, we discuss the prognostic value of ferroptosis-related genes (FRGs), their association with immune infiltration, and their implications for personalized immunotherapy. Collectively, these insights emphasize the translational promise of targeting ferroptosis as a novel strategy for precision oncology and targeted therapy in cervical cancer.